Nimodipine has no effect on the cerebral circulation in conscious pigs, despite an increase in cardiac output

Giessen, Willem J. van der; Duncker, Dirk J.; Saxena, Pramod R.; Verdouw, Pieter D.

doi:10.1111/j.1476-5381.1990.tb15795.x

Cited by 7 publications

(9 citation statements)

References 43 publications

(51 reference statements)

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“…3); 6 of these studies were conducted in animals. [54][55][56]59,60,62 The majority of the human studies were small cohort and case-control studies; the largest included 314 participants. None of the included studies were randomized controlled trials, and all were at high risk of bias across all domains (Selection, Performance, Detection, Attrition, and Reporting) per the Cochrane guidelines.…”

Section: Resultsmentioning

confidence: 99%

“…None of the included studies were randomized controlled trials, and all were at high risk of bias across all domains (Selection, Performance, Detection, Attrition, and Reporting) per the Cochrane guidelines. 27 Methods of measuring CBF included cerebral artery mean velocity [28][29][30][31][32][33][34][35][36][37][38][39][40][41][42][43][44][45][46] and mean flow assessed using transcranial Doppler (TCD) sonography, 47,48,[50][51][52] radiotracers, [53][54][55][56][57][58][59][60][61][62][63]68 magnetic resonance perfusion, [64][65][66] thermal diffusion flowmetry, 49 and jugular venous oximetry. 67 CO was also measured in a variety of ways including with thermodilution through right-heart catheterization, 29,34,44,45,...…”

Section: Resultsmentioning

confidence: 99%

“…real time cardiac imaging (echocardiography and magnetic resonance imaging), 31,48,51,65,66 aortic flow, 56 impedance cardiography, 39,41,43 and inert gas rebreathing techniques. 38,42 Results were heterogenous, with both corroboration and confutation of a relationship between CO and CBF in both normal and abnormal cerebrovascular states.…”

Section: Resultsmentioning

confidence: 99%

“…The effect on CBF of multiple vasoactive agents, including dobutamine, 34,[43][44][45]48,58 olprinone, 49 norepinephrine, 33,46 nimodipine, 56 phenylephrine, 53 and isoprenaline, 54 were analyzed. CBF was primarily measured with TCD 33,34,[43][44][45][46]48 and radiotracers 53,54,56,58 34,44,45,48 and was associated with increases in middle cerebral artery flow velocity (Vmca) 34,44,45 ; however, PaCO 2 was inconsistently controlled in these studies.…”

Section: Vasoactive Agentsmentioning

confidence: 99%

Section: Vasoactive Agentsmentioning

confidence: 99%

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Cardiac Output and Cerebral Blood Flow: A Systematic Review of Cardio-Cerebral Coupling

Castle-Kirszbaum¹,

Parkin

Goldschlager³

et al. 2021

Journal of Neurosurgical Anesthesiology

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Control of cerebral blood flow (CBF) is crucial to the management of neurocritically ill patients. Small studies which have examined the role of cardiac output (CO) as a determinant of CBF have inconsistently demonstrated evidence of cardio-cerebral coupling. Putative physiological mechanisms underpinning such coupling include changes in arterial blood pressure pulsatility, which would produce vasodilation through increased oscillatory wall-shear-stress and baroreceptor mediated reflex sympatholysis, and changes in venous backpressure which may improve cerebral perfusion pressure. We sought to summarize and contextualize the literature on the relationship between CO and CBF and discuss the implications of cardio-cerebral coupling for neurocritical care. A systematic review of the literature yielded 41 studies; all were of low-quality and at high-risk of bias. Results were heterogenous, with evidence for both corroboration and confutation of a relationship between CO and CBF in both normal and abnormal cerebrovascular states. Common limitations of studies were lack of instantaneous CBF measures with reliance on transcranial Doppler–derived blood flow velocity as a surrogate, inability to control for fluctuations in established determinants of CBF (eg, PaCO2), and direct effects on CBF by the interventions used to alter CO. Currently, the literature is insufficiently robust to confirm an independent relationship between CO and CBF. Hypothetically, the presence of cardio-cerebral coupling would have important implications for clinical practice. Manipulation of CBF could occur without the risks associated with extremes of arterial pressure, potentially improving therapy for those with cerebral ischemia of various etiologies. However, current literature is insufficiently robust to confirm an independent relationship between CO and CBF, and further studies with improved methodology are required before therapeutic interventions can be based on cardio-cerebral coupling.

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